3. Analysis of a compensatory response. Metabolic disorders result in compensatory changes in ventilation and thus in PCO2, whereas respiratory disorders result in compensatory changes in RNAE and thus in ECF [HCO3 −] (
Table 37.2 ). In an appropriately compensated metabolic acidosis, the PCO2 is decreased, whereas it is elevated in compensated metabolic alkalosis. With respiratory acidosis, compensation results in an elevation of the [HCO3 −]. Conversely, ECF [HCO3 −] is reduced in response to respiratory alkalosis. In this example, the PCO2 is reduced from normal, and the magnitude of this reduction (10 mm Hg decrease in PCO2 for an 8 mEq/L decrease in ECF [HCO3 −]) is as expected (see
Table 37.2 ). Therefore the acid-base disorder is a simple metabolic acidosis with appropriate respiratory compensation. A mixed acid-base disorder reflects the presence of two or more underlying causes for the acid-base disturbance. For example, consider the following data: pH = .6 96
When the three-step approach is followed, it is evident that the disturbance is an acidosis that has both a metabolic component (ECF [HCO3 −] < 24 mEq/L) and a respiratory component (PCO2 > 40 mm Hg). Thus this disorder is mixed. Mixed acid-base disorders can occur, for example, in an individual who has a history of a chronic pulmonary disease such as emphysema (i.e., chronic respiratory acidosis) and who develops an acute gastrointestinal illness with diarrhea. Because diarrhea fluid contains HCO3 − , its loss from the body results in the development of metabolic acidosis.
A mixed acid-base disorder is also indicated when a patient has abnormal PCO2 and ECF [HCO3 −] values but the pH is normal. Such a condition can develop in a patient who has ingested a large quantity of aspirin. Salicylic acid (active ingredient in aspirin) produces metabolic acidosis and at the same time stimulates the respiratory centers, causing hyperventilation and respiratory alkalosis. Thus the patient has a reduced ECF [HCO3 −] and a reduced PCO2. (NOTE: The PCO2 is lower than would occur with normal respiratory compensation of a metabolic acidosis.) 1.
The kidneys maintain acid-base balance through excretion of an amount of acid equal to the amount of nonvolatile acid produced by metabolism and the quantity ingested in the diet (termed renal net acid excretion [RNAE]). The kidneys also prevent loss of HCO3 − in urine by reabsorbing virtually all the HCO3 − filtered at the glomeruli. Both reabsorption of filtered HCO3 − and excretion of acid are accomplished by secretion of H+ by the nephrons. Acid is excreted by the kidneys in the form of titratable acid (primarily as Pi) and NH4 + . Both titratable acid and NH4 + excretion result in generation of new HCO3 − , which replenishes the ECF HCO3 − lost during neutralization of nonvolatile acids.
2.
The body uses three lines of defense to minimize the impact of acid-base disorders on body fluid pH: (1) ECF and ICF buffering, (2) respiratory compensation, and (3) renal compensation.
Curthoys NP. Renal ammonium ion production and excretion. In: Alpern RJ, et al., eds. Seldin and Giebisch’s The Kidney: Physiology and Pathophysiology. 5th ed. Waltham, MA: Elsevier; 2013.
Dubose TD Jr. Disorders of acid-base balance. In: Taal MW, et al., eds. Brenner and Rector’s The Kidney. 9th ed. Philadelphia: Saunders; 2012.